Dipyridamole enhances angiotensin II-induced arterial relaxation by increasing PGI2 production and smooth muscle sensitivity, overcoming prostaglandin synthesis inhibition.
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Animal data on dipyridamole warrant no practice change; leaves open human translation of prostaglandin-mediated vascular effects.
Angiotensin (ANG) ll-induced relaxations in isolated dog renal and cerebral arteries are postulated to be mediated by the release of prostaglandin (PG) l2 from the arterial wall. In helical strips of dog renal arteries treated with dipyridamole, relaxations induced by ANG II (10−7 M) and exogenously applied PGI2 (10−8 M) were potentiated; the potentiation was appreciably greater in the ANG-induced relaxation. Treatment with phthalazinol did not alter the response to ANG II, but significantly potentiated the relaxation induced by PGI2. The ANG-induced relaxations were suppressed or reversed to contractions by aspirin or indomethacin. Combined treatment of dipyridamole with aspirin or indomethacin restored the relaxant response to ANG II, while phthalazinol in combination with aspirin did not restore the response. It may be concluded that the potentiation of responses to ANG II by dipyridamole is associated with increments in the release of PGI2 from the arterial wall and potentiations of the response of arterial smooth muscle to PGI2. Dipyridamole appears to increase the production of PGI2 even in the presence of PG synthesis inhibition by aspirin or indomethacin.
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Toda et al. (1983) studied this question.
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